Yeah! Er strahlt ☢️ gerade bis über beide Ohren
https://www.sciencedirect.com/science/article/pii/S2211383526004235
https://www.sciencedirect.com/science/article/pii/S2211383526004235
👍5❤2👏2
Nochmal für mein Verständnis: Wir bekommen ein GANZES Kapitel! GEDRUCKT! In Hochglanz! 50 verdammte Seiten in einem Q1-JOURNAL!
https://www.sciencedirect.com/science/article/pii/S2211383526004235#bib285
https://www.sciencedirect.com/science/article/pii/S2211383526004235#bib285
🏆13🆒1
Electronegativity-Driven Structured Environments in DNA and RNA: Vibronic Coupling, Quantum Overlays, and Nucleic Acid Dynamics—A Perspective
https://www.mdpi.com/2624-960X/8/3/64
https://www.mdpi.com/2624-960X/8/3/64
MDPI
Electronegativity-Driven Structured Environments in DNA and RNA: Vibronic Coupling, Quantum Overlays, and Nucleic Acid Dynamics—A…
Nucleic acids exhibit structured electromagnetic features shaped by classical electronegativity (EN) patterns. Mapping Pauling EN values across DNA and RNA reveals a largely invariant, high-EN phosphodiester backbone that provides a consistent electrostatic…
👍1
https://www.trialsitenews.com/a/are-lipid-nanoparticles-really-inert-new-review-raises-a-serious-mechanistic-question-4bc482ed
Musste TSN korrigieren. Ich hoffe mein Kommentar wird angezeigt:
"Dear TrialSite News Editorial Team,
Thank you for covering our review. I would, however, like to clarify one central aspect of our hypothesis, as it is presented somewhat inaccurately in your article.
You state that our review describes "possible downstream effects involving ... phosphoinositide signaling." This is, however, not the central hypothesis of our review.
Rather, our proposed L-DMD model postulates that perturbation of the phosphatidylinositol (PI) cycle, or more broadly phosphoinositide homeostasis, constitutes the primary membrane-level event. The downstream signaling pathways–including NF-kB, MAPK, JAK/STAT, PI3K/AKT/mTOR, PLC-mediated calcium signaling, and others–are interpreted in our model as consequences of this primary membrane dysregulation, rather than as independent parallel findings.
The rationale for this hierarchy is rooted in the electrostatic and dielectric properties of biological membranes. Our hypothesis is that ionizable lipids, by transiently integrating into cellular and endosomal membranes, alter membrane electrostatics, lipid packing, and the spatial organization of phosphoinositide pools. Since phosphoinositides function as membrane-localized organizers of signaling complexes, perturbation of their homeostasis is expected to propagate through numerous downstream pathways. Thus, in our model, phosphoinositide dysregulation is not simply one signaling event among many, but the upstream membrane-centered mechanism from which the subsequent signaling alterations arise.
A specific example illustrates this distinction. In the case of TLR4 signaling, our hypothesis is not that ionizable lipids merely activate the receptor directly. Rather, we propose that membrane perturbations affecting phosphoinositide microdomains, particularly PI(4,5)P₂-dependent membrane organization, may alter receptor localization, orientation, and signaling bias. The observed MyD88/TRIF imbalance is therefore interpreted as a downstream consequence of altered membrane architecture, not as an independent primary event.
This mechanistic framework is developed from established membrane biology, the physicochemical properties of ionizable lipids, and the understanding of LNPs as supramolecular assemblies.
As stated explicitly in the Abstract, our hypothesis is that "the phosphatidylinositol (PI) cycle is the primary site of LNP-induced perturbations," the disruption of which subsequently "triggers downstream signaling cascades" that give rise to the observed network-level alterations.
This mechanistic hierarchy–membrane/PI-cycle perturbation -> downstream signaling network dysregulation–constitutes the central conceptual framework of our review.
Kind regards,
Falko Seger(First Author)"
Musste TSN korrigieren. Ich hoffe mein Kommentar wird angezeigt:
"Dear TrialSite News Editorial Team,
Thank you for covering our review. I would, however, like to clarify one central aspect of our hypothesis, as it is presented somewhat inaccurately in your article.
You state that our review describes "possible downstream effects involving ... phosphoinositide signaling." This is, however, not the central hypothesis of our review.
Rather, our proposed L-DMD model postulates that perturbation of the phosphatidylinositol (PI) cycle, or more broadly phosphoinositide homeostasis, constitutes the primary membrane-level event. The downstream signaling pathways–including NF-kB, MAPK, JAK/STAT, PI3K/AKT/mTOR, PLC-mediated calcium signaling, and others–are interpreted in our model as consequences of this primary membrane dysregulation, rather than as independent parallel findings.
The rationale for this hierarchy is rooted in the electrostatic and dielectric properties of biological membranes. Our hypothesis is that ionizable lipids, by transiently integrating into cellular and endosomal membranes, alter membrane electrostatics, lipid packing, and the spatial organization of phosphoinositide pools. Since phosphoinositides function as membrane-localized organizers of signaling complexes, perturbation of their homeostasis is expected to propagate through numerous downstream pathways. Thus, in our model, phosphoinositide dysregulation is not simply one signaling event among many, but the upstream membrane-centered mechanism from which the subsequent signaling alterations arise.
A specific example illustrates this distinction. In the case of TLR4 signaling, our hypothesis is not that ionizable lipids merely activate the receptor directly. Rather, we propose that membrane perturbations affecting phosphoinositide microdomains, particularly PI(4,5)P₂-dependent membrane organization, may alter receptor localization, orientation, and signaling bias. The observed MyD88/TRIF imbalance is therefore interpreted as a downstream consequence of altered membrane architecture, not as an independent primary event.
This mechanistic framework is developed from established membrane biology, the physicochemical properties of ionizable lipids, and the understanding of LNPs as supramolecular assemblies.
As stated explicitly in the Abstract, our hypothesis is that "the phosphatidylinositol (PI) cycle is the primary site of LNP-induced perturbations," the disruption of which subsequently "triggers downstream signaling cascades" that give rise to the observed network-level alterations.
This mechanistic hierarchy–membrane/PI-cycle perturbation -> downstream signaling network dysregulation–constitutes the central conceptual framework of our review.
Kind regards,
Falko Seger(First Author)"
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Lipidnanopartikel und Metastabilität.pdf
98 KB
Wenn eine KI deine Kritik an LNPs härter bewertet als TrialSite News... LOOOOOOOOOOL!
https://www.trialsitenews.com/a/are-lipid-nanoparticles-really-inert-new-review-raises-a-serious-mechanistic-question-4bc482ed
https://www.trialsitenews.com/a/are-lipid-nanoparticles-really-inert-new-review-raises-a-serious-mechanistic-question-4bc482ed
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Forwarded from Tom Lausen ‼️❗️original Datenanalyst
LESEEMPFEHLUNG
Die beste Arbeit seit längerer Zeit. Die Risikohochstufung des "vergesslichen" Chefs des RKI - Lars Schaade und seinem Kollegen Lothar Wieler und wie ein Puzzle langsam das Bild sichtbarer macht.
Tolle Arbeit und es ist noch lange nicht alles aufgeklärt, aber es wird immer mehr. Für unsere Kinder und die Generationen danach wird es wichtig sein.
https://multipolar-magazin.de/artikel/die-menschen-sollen-angst-haben
Die beste Arbeit seit längerer Zeit. Die Risikohochstufung des "vergesslichen" Chefs des RKI - Lars Schaade und seinem Kollegen Lothar Wieler und wie ein Puzzle langsam das Bild sichtbarer macht.
Tolle Arbeit und es ist noch lange nicht alles aufgeklärt, aber es wird immer mehr. Für unsere Kinder und die Generationen danach wird es wichtig sein.
https://multipolar-magazin.de/artikel/die-menschen-sollen-angst-haben
Mutflash - Medizinische Argumentationen und Studiensammlungen
https://tkp.at/2026/07/03/weisse-faserklumpen-dokumentiert-von-808-leichenbestattern-in-fuenf-laendern/
Komatsuya K, Kaneko K, Kasahara K. Function of Platelet Glycosphingolipid Microdomains/Lipid Rafts. Int J Mol Sci. 2020 Aug 2;21(15):5539. doi: 10.3390/ijms21155539. PMID: 32748854; PMCID: PMC7432685.
Miron-Mendoza M, Vazquez D, García-Rámila N, Ikebe HR, Petroll WM. Coupling of Fibrin Reorganization and Fibronectin Patterning by Corneal Fibroblasts in Response to PDGF BB and TGFβ1. Bioengineering (Basel). 2020 Aug 7;7(3):89. doi: 10.3390/bioengineering7030089. PMID: 32784578; PMCID: PMC7552779.
Hm... Wenn unsere Hypothese korrekt ist... Ouch!
Miron-Mendoza M, Vazquez D, García-Rámila N, Ikebe HR, Petroll WM. Coupling of Fibrin Reorganization and Fibronectin Patterning by Corneal Fibroblasts in Response to PDGF BB and TGFβ1. Bioengineering (Basel). 2020 Aug 7;7(3):89. doi: 10.3390/bioengineering7030089. PMID: 32784578; PMCID: PMC7552779.
Hm... Wenn unsere Hypothese korrekt ist... Ouch!
Mutflash - Medizinische Argumentationen und Studiensammlungen
Komatsuya K, Kaneko K, Kasahara K. Function of Platelet Glycosphingolipid Microdomains/Lipid Rafts. Int J Mol Sci. 2020 Aug 2;21(15):5539. doi: 10.3390/ijms21155539. PMID: 32748854; PMCID: PMC7432685. Miron-Mendoza M, Vazquez D, García-Rámila N, Ikebe HR…
Nachbemerkung
Falls unser Rahmenwerk zutrifft, wäre zu erwarten, dass eine Störung der phosphoinositidabhängigen Membransignalübertragung zahlreiche miteinander verknüpfte Prozesse beeinflusst, darunter die Thrombozytenaktivierung, die Organisation von Lipid-Rafts, die Integrin-Signalübertragung, die MAPK-abhängige Regulation sowie das Remodeling von Fibrin und Fibronectin. Dies liefert einen biologisch plausiblen mechanistischen Rahmen, der zur Entstehung ungewöhnlicher thrombotischer Phänotypen beitragen könnte. Ob dies jedoch ausreicht, um spezifische pathologische Befunde zu erklären, muss experimentell geklärt werden.
Komatsuya et al. (2020) zeigen, dass die Funktion von Thrombozyten entscheidend von glycosphingolipidreichen Lipid-Rafts und Membranmikrodomänen abhängt. Diese Mikrodomänen organisieren nicht nur die Signalübertragung innerhalb der Thrombozyten selbst, sondern koordinieren auch Rezeptorinteraktionen an der Grenzfläche zwischen Thrombozyten und ihren Interaktionspartnern, einschließlich Endothelzellen, Leukozyten und Komponenten der extrazellulären Matrix. Dies steht im Einklang mit unserer zentralen Annahme, dass die Membranorganisation kein passives strukturelles Merkmal ist, sondern ein aktiver Determinant der Signalverarbeitung.
Komatsuya K, Kaneko K, Kasahara K. Function of Platelet Glycosphingolipid Microdomains/Lipid Rafts. Int J Mol Sci. 2020 Aug 2;21(15):5539. doi:10.3390/ijms21155539. PMID: 32748854; PMCID: PMC7432685
Miron-Mendoza et al. zeigten darüber hinaus, dass die durch PDGF und TGF-β vermittelte Signalübertragung die koordinierte Organisation von Fibrin und Fibronectin reguliert. Dies unterstreicht, dass die Architektur der extrazellulären Matrix nicht allein von der Menge der vorhandenen Proteine bestimmt wird, sondern ebenso von den zugrunde liegenden Signalnetzwerken, welche deren Zusammenbau und kontinuierliches Remodeling steuern.
Miron-Mendoza M, Vazquez D, García-Rámila N, Ikebe HR, Petroll WM. Coupling of Fibrin Reorganization and Fibronectin Patterning by Corneal Fibroblasts in Response to PDGF BB and TGFβ1. Bioengineering (Basel). 2020 Aug 7;7(3):89. doi:10.3390/bioengineering7030089. PMID: 32784578; PMCID: PMC7552779.
https://substack.com/@genervter/note/c-292060920
Falls unser Rahmenwerk zutrifft, wäre zu erwarten, dass eine Störung der phosphoinositidabhängigen Membransignalübertragung zahlreiche miteinander verknüpfte Prozesse beeinflusst, darunter die Thrombozytenaktivierung, die Organisation von Lipid-Rafts, die Integrin-Signalübertragung, die MAPK-abhängige Regulation sowie das Remodeling von Fibrin und Fibronectin. Dies liefert einen biologisch plausiblen mechanistischen Rahmen, der zur Entstehung ungewöhnlicher thrombotischer Phänotypen beitragen könnte. Ob dies jedoch ausreicht, um spezifische pathologische Befunde zu erklären, muss experimentell geklärt werden.
Komatsuya et al. (2020) zeigen, dass die Funktion von Thrombozyten entscheidend von glycosphingolipidreichen Lipid-Rafts und Membranmikrodomänen abhängt. Diese Mikrodomänen organisieren nicht nur die Signalübertragung innerhalb der Thrombozyten selbst, sondern koordinieren auch Rezeptorinteraktionen an der Grenzfläche zwischen Thrombozyten und ihren Interaktionspartnern, einschließlich Endothelzellen, Leukozyten und Komponenten der extrazellulären Matrix. Dies steht im Einklang mit unserer zentralen Annahme, dass die Membranorganisation kein passives strukturelles Merkmal ist, sondern ein aktiver Determinant der Signalverarbeitung.
Komatsuya K, Kaneko K, Kasahara K. Function of Platelet Glycosphingolipid Microdomains/Lipid Rafts. Int J Mol Sci. 2020 Aug 2;21(15):5539. doi:10.3390/ijms21155539. PMID: 32748854; PMCID: PMC7432685
Miron-Mendoza et al. zeigten darüber hinaus, dass die durch PDGF und TGF-β vermittelte Signalübertragung die koordinierte Organisation von Fibrin und Fibronectin reguliert. Dies unterstreicht, dass die Architektur der extrazellulären Matrix nicht allein von der Menge der vorhandenen Proteine bestimmt wird, sondern ebenso von den zugrunde liegenden Signalnetzwerken, welche deren Zusammenbau und kontinuierliches Remodeling steuern.
Miron-Mendoza M, Vazquez D, García-Rámila N, Ikebe HR, Petroll WM. Coupling of Fibrin Reorganization and Fibronectin Patterning by Corneal Fibroblasts in Response to PDGF BB and TGFβ1. Bioengineering (Basel). 2020 Aug 7;7(3):89. doi:10.3390/bioengineering7030089. PMID: 32784578; PMCID: PMC7552779.
https://substack.com/@genervter/note/c-292060920
❤2
Let's sing a song!
♪♫♫♪
Spike, Spike, Spike
Spike, Spike, Spike, the nasty protein,
Perfect boogeyman we can sell on the screen.
Spike, Spike, Spike
Who needs LNPs when you’ve got Spike, Spike, Spike?
No more of those tiny packages causing a strike.
Spike, Spike, Spike
Sing it loud, let the chorus grow,
A little spark and away we go.
Spike, Spike, Spike
So reach for the cure, the grand new phase,
Apharese dreams in a neon haze.
Spike, Spike, Spike
Add a dash of growth, let the future unfold,
A story of power, a tale retold.
Spike, Spike, Spike
Soon the symptoms fade from sight…
Or so they promised through the night.
Spike, Spike, Spike
The voices cheer, the banners rise,
While shadows gather under skies.
Spike, Spike, Spike,
The sweetest song with the sharpest bite.
A melody dressed in golden light,
Spike, Spike, Spike
And when the final echoes break,
When no more claims remain to make,
Spike, Spike, Spike
One question hangs beneath the sky:
Was it the spark that made us fly?
Spike, Spike, Spike
Was it the dream we couldn’t see?
Was it the thing that set us free?
Spike, Spike, Spike
Alive or gone, it’s all the same –
No one remembers who’s to blame.
Spike, Spike, Spike
The lights go out. The records fade.
The final note is softly played.
Spike, Spike, Spike
Livend or dead, the truth remains:
The Spike was there… and left its stains.
Spike, Spike, Spike, nana, na, na naa!
♪♫♪♫
♪♫♫♪
Spike, Spike, Spike
Spike, Spike, Spike, the nasty protein,
Perfect boogeyman we can sell on the screen.
Spike, Spike, Spike
Who needs LNPs when you’ve got Spike, Spike, Spike?
No more of those tiny packages causing a strike.
Spike, Spike, Spike
Sing it loud, let the chorus grow,
A little spark and away we go.
Spike, Spike, Spike
So reach for the cure, the grand new phase,
Apharese dreams in a neon haze.
Spike, Spike, Spike
Add a dash of growth, let the future unfold,
A story of power, a tale retold.
Spike, Spike, Spike
Soon the symptoms fade from sight…
Or so they promised through the night.
Spike, Spike, Spike
The voices cheer, the banners rise,
While shadows gather under skies.
Spike, Spike, Spike,
The sweetest song with the sharpest bite.
A melody dressed in golden light,
Spike, Spike, Spike
And when the final echoes break,
When no more claims remain to make,
Spike, Spike, Spike
One question hangs beneath the sky:
Was it the spark that made us fly?
Spike, Spike, Spike
Was it the dream we couldn’t see?
Was it the thing that set us free?
Spike, Spike, Spike
Alive or gone, it’s all the same –
No one remembers who’s to blame.
Spike, Spike, Spike
The lights go out. The records fade.
The final note is softly played.
Spike, Spike, Spike
Livend or dead, the truth remains:
The Spike was there… and left its stains.
Spike, Spike, Spike, nana, na, na naa!
♪♫♪♫
👍2🤪2❤1
Puh... Gott sei Dank gibt es noch ein paar kritisch denkende Menschen.
https://x.com/MeganSuspended/status/2075058575618244727
https://x.com/MeganSuspended/status/2075546891488579809
https://x.com/MeganSuspended/status/2075058575618244727
https://x.com/MeganSuspended/status/2075546891488579809
Galley Proof ist da... Hochdruck! 48 Stunden... -_- Die haben unsere Table 2 zerschrottet... :-S Das müssen wir erstmal gerade biegen.
Und ich mag es nicht wirklich, wo die die Figuren so verstreut haben. Aber egal. Narf!
Und ich mag es nicht wirklich, wo die die Figuren so verstreut haben. Aber egal. Narf!